During normal cardiac function, the ventricles fill during two diastolic phases, a passive filling phase and an active filling phase. The passive filling phase occurs first as the ventricles relax following ventricular systole. Ventricular relaxation causes the pressure within the ventricles to fall, allowing the mitral valve between the left atrium and left ventricle and the tricuspid valve between the right atrium and right ventricle to open. Blood flows into the ventricular chambers during the passive filling phase due to the pressure difference across the mitral and tricuspid valves. As the passive filling rate slows, the atria contract, actively contributing the ventricular filling. The force generated by the actively contracting atria forces more blood into the ventricle that has already filled passively.
This atrial contribution to ventricular filling is important in maintaining an adequate preload for optimal ventricular contraction. According to the Frank-Starling law, the ventricles contract more forcefully during systole when filled to a greater degree during diastole. Generally, cardiac stroke volume increases as cardiac filling increases.
The atrial contribution to ventricular filling can become compromised during many disease states. Cardiac conditions that alter the relative timing of atrial and ventricular contraction may reduce the atrial contribution to ventricular filling, and thereby reduce the overall cardiac output. If atrial contraction occurs too late after the passive filling phase, ventricular contraction may have already begun, closing the mitral or tricuspid valves. Thus, late atrial contraction may cause the atria to contract against a closed or partially closed valve, which can result in retrograde flow. Early atrial contraction, prior to the end of the passive filling phase, results in fusion of the passive and active filling phases. The force available from the contracting atria is under utilized when blood is forced into an empty or only partially filled ventricle. Overall filling is reduced.
During a number of cardiac stimulation therapies, including dual chamber pacing, cardiac resynchronization therapy, extra-systolic stimulation, among others, an atrial-ventricular (AV) delay is set to control the timing between atrial depolarization and ventricular depolarization. The AV delay can be optimized based on various hemodynamic measurements. For example, the AV delay can be optimized using echocardiography for maximizing a measured ejection fraction or other hemodynamic or cardiac function metric. However, performing such echocardiography studies are generally time consuming and require skilled personnel to program the implantable cardiac stimulation device, such as a pacemaker or implantable cardioverter defibrillator (ICD), to multiple AV delay settings and to perform the echocardiography measurements. Furthermore, an AV delay setting determined to be optimal during an office visit may change over time with disease state or changes in patient activity level, medications or other influences. In order to achieve the full hemodynamic benefits of various cardiac stimulation therapies, it is desirable to be able to monitor atrial function such that the active, atrial contribution to ventricular filling is optimized. Monitoring the atrial function is also useful in monitoring a disease state.